Journal
VACCINES
Volume 9, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/vaccines9060655
Keywords
Epstein-Barr virus (EBV); Kaposi sarcoma associated herpesvirus (KSHV); NKG2D; NKG2A; DNAM-1
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Funding
- Cancer Research Switzerland [KFS4091-02-2017, KFS-4962-02-2020]
- Cancer Research Center Zurich
- Vontobel Foundation
- Sobek Foundation
- Swiss Vaccine Research Institute
- Roche
- Swiss National Science Foundation [310030B_182827, 310030L_197952/1, CRSII5_180323]
- Novartis
- KFSP-PrecisionMS and HMZ ImmunoTargET of the University of Zurich
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Herpesviruses play a key role in shaping NK cell repertoires, with CMV driving NKG2C-positive NK cell accumulation and EBV expanding NKG2A-positive NK cells. While adaptive NK cells support immunity through antibody-dependent cellular cytotoxicity, NKG2A-positive NK cells seem to target lytic EBV replicating B cells. The importance of restricting EBV replication during gamma-herpesvirus pathogenesis will be discussed, along with summarizing the impact of coinfections on EBV-driven NK cell expansion.
Herpesviruses are main sculptors of natural killer (NK) cell repertoires. While the beta-herpesvirus human cytomegalovirus (CMV) drives the accumulation of adaptive NKG2C-positive NK cells, the human gamma-herpesvirus Epstein-Barr virus (EBV) expands early differentiated NKG2A-positive NK cells. While adaptive NK cells support adaptive immunity by antibody-dependent cellular cytotoxicity, NKG2A-positive NK cells seem to preferentially target lytic EBV replicating B cells. The importance of this restriction of EBV replication during gamma-herpesvirus pathogenesis will be discussed. Furthermore, the modification of EBV-driven NK cell expansion by coinfections, including by the other human gamma-herpesvirus Kaposi sarcoma-associated herpesvirus (KSHV), will be summarized.
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